ABSTRACT
The QT interval has been studied in ECG in mouse and rat embryos during two stages of development. The QT interval during the early stage of development is prolonged and an ST segment clearly exists. Both disappear during fetal development and do not exist in adult animals in which the T wave immediately follows the QRS. Mammalian embryos have therefore been proposed as a model for the study of QT prolongation. It is suggested that the origin of the QT prolongation in the young embryos is caused by the prolonged duration of the action potentials of the primordial cardiac tissue. During embryonic development this tissue becomes organized as a conductive system surrounded by "neomyocardial" tissue with a shorter duration of action potential, which causes the shorter QT interval at this stage. Our working hypothesis is that the pathogenesis of the prolonged QT syndrome in children could be interpreted as an incomplete or delayed differentiation between the primordial or primordial-like myocardium retaining prolonged action potential duration, and "neomyocardium" with short duration.
